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Cancer Microenviron. 2010 Feb 27;3(1):97-105. doi: 10.1007/s12307-010-0043-6.

Selectins as mediators of lung metastasis.

Author information

  • 1Institute of Physiology, Zürich Center for Integrative Human Physiology, University of Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland.

Abstract

Lung metastasis remains the major cause of cancer related mortality in patients with breast, gastrointestinal, sarcoma, melanoma and kidney cancer. Here we characterize the expression of selectins during metastatic lung colonization and analyzed their function in the formation of pulmonary metastasis. E-selectin, together with VCAM-1, were detected 6 h after the microvascular arrest of tumor cells indicating an inflammatory activation of the local endothelial cells. No E-selectin expression was detected in pre-metastatic lungs of mice carrying primary tumors. P- and L-selectin were present during initiating steps of lung colonization and correlated with the recruitment of platelets and leukocytes to metastatic tumor cells. Experimental metastasis was significantly reduced in the absence of P- or L-selectin while no attenuation of metastasis was observed in E-selectin-deficient mice. Collectively, selectins are upregulated within the metastatic microenvironment of tumor cells and the formation of a permissive metastatic microenvironment is facilitated by P- and L-selectin mediated interactions between tumor cells and blood components. E-selectin does not affect metastatic initiation in the lung tissue and its expression rather indicates a local activation of lung microvascular endothelial cells.

ELECTRONIC SUPPLEMENTARY MATERIAL:

The online version of this article (doi:10.1007/s12307-010-0043-6) contains supplementary material, which is available to authorized users.

KEYWORDS:

Carcinomas; Endothelium; Metastasis; Metastatic microenvironment; Selectins; Tumor microenvironment

PMID:
21209777
[PubMed]
PMCID:
PMC2990482
Free PMC Article

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